The effects of caffeine and Ca2+ on rigor tension in triton-treated rat ventricular trabeculae

1992 ◽  
Vol 421 (4) ◽  
pp. 343-349 ◽  
Author(s):  
D. S. Steele ◽  
G. L. Smith
Keyword(s):  
Rigor Tension ◽  
Ventricular Trabeculae

Contractile effects of cardiac neuropeptides in isolated canine atrial and ventricular muscles

1989 ◽  
Vol 257 (4) ◽  
pp. H1082-H1087 ◽  
Author(s):  
D. F. Rigel ◽  
I. L. Grupp ◽  
A. Balasubramaniam ◽  
G. Grupp
Keyword(s):  
Isometric Force ◽  
Contractile Force ◽  
Adrenergic Blockade ◽  
Canine Heart ◽  
Inotropic Action ◽  
Inotropic Effects ◽  
Calcitonin Gene ◽  
Positive Inotropic Effects ◽  
The Right ◽  
Ventricular Trabeculae

Contractile effects of the cardiac neuropeptides vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and neurotensin (NT) were compared with those of l-isoproterenol (ISO) in isolated canine atrial and ventricular trabeculae muscles stimulated to contract at 1 Hz. In ventricular muscles, ISO, VIP, and PHI augmented developed isometric force by approximately 100%. VIP and PHI were three times and 1/10, respectively, as potent as ISO. VIP also exhibited positive inotropic effects in atrial trabeculae. The contractile responses to VIP were unchanged after beta-adrenergic blockade with nadolol at a concentration (10 microM) that shifted the ISO dose-response curve two to three orders of magnitude to the right. In atrial and ventricular trabeculae, NPY (1 microM) attenuated contractile force by 36 +/- 8 and 30 +/- 4%, respectively. Each peptide also caused comparable increases or decreases in the rate of development of force and the rate of relaxation. CGRP and NT caused no significant changes in developed force in either atrial or ventricular muscles in concentrations up to 1 microM. Our results indicate a potential positive inotropic action of endogenous VIP and PHI and a cardiodepressant effect of endogenous NPY in the canine heart.

scholarly journals The Orientation of the H1 and H2 Helices of Troponin I in Ventricular Trabeculae

2009 ◽  
Vol 96 (3) ◽  
pp. 229a
Author(s):  
Nadia Caro-Goldrine ◽  
Yin-Biao Sun ◽  
David R. Trentham ◽  
Malcolm Irving
Keyword(s):  
Troponin I ◽  
Ventricular Trabeculae

scholarly journals Stretch and quick release of rat cardiac trabeculae accelerates Ca2+ waves and triggered propagated contractions

2001 ◽  
Vol 281 (5) ◽  
pp. H2133-H2142 ◽  
Author(s):  
Yuji Wakayama ◽  
Masahito Miura ◽  
Yoshinao Sugai ◽  
Yutaka Kagaya ◽  
Jun Watanabe ◽  
...  
Keyword(s):  
Strain Gauge ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Laser Diffraction ◽  
Active Force ◽  
Quick Release ◽  
Rat Hearts ◽  
Initiation And Propagation ◽  
Intracellular Ca ◽  
Ventricular Trabeculae

Rapid shortening of active cardiac muscle [quick release (QR)] dissociates Ca2+ from myofilaments. We studied, using muscle stretches and QR, whether Ca2+ dissociation affects triggered propagated contractions (TPCs) and Ca2+waves. The intracellular Ca2+ concentration was measured by a SIT camera in right ventricular trabeculae dissected from rat hearts loaded with fura 2 salt, force was measured by a silicon strain gauge, and sarcomere length was measured by laser diffraction while a servomotor controlled muscle length. TPCs ( n = 27) were induced at 28°C by stimulus trains (7.5 s at 2.65 ± 0.13 Hz) at an extracellular Ca2+ concentration ([Ca2+]o) = 2.0 mM or with 10 μM Gd3+ at [Ca2+]o = 5.2 ± 0.73 mM. QR during twitch relaxation after a 10% stretch for 100–200 ms reduced both the time between the last stimulus and the peak TPC (PeakTPC) and the time between the last stimulus and peak Ca2+ wave (PeakCW) and increased PeakTPC and PeakCW ( n= 13) as well as the propagation velocity ( V prop; n = 8). Active force during stretch also increased V prop( r = 0.84, n = 12, P < 0.01), but Gd3+ had no effect ( n = 5). These results suggest that Ca2+ dissociation by QR during relaxation accelerates the initiation and propagation of Ca2+ waves.

Increased ventricular stiffness and decreased cardiac function in Atlantic cod (Gadus morhua) at high temperatures

2013 ◽  
Vol 305 (8) ◽  
pp. R864-R876 ◽  
Author(s):  
Douglas A. Syme ◽  
A. Kurt Gamperl ◽  
Gordon W. Nash ◽  
Kenneth J. Rodnick
Keyword(s):  
Stroke Volume ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Isometric Force ◽  
Full Range ◽  
Large Strains ◽  
High Heart Rate ◽  
Ventricular Filling ◽  
Ventricular Trabeculae

We employed the work loop method to study the ability of ventricular and atrial trabeculae from Atlantic cod to sustain power production during repeated contractions at acclimation temperatures (10°C) and when acutely warmed (20°C). Oxygen tension (Po2) was lowered from 450 to 34% air saturation to augment the thermal stress. Preparations worked under conditions simulating either a large stroke volume (35 contractions/min rate, 8–12% muscle strain) or a high heart rate (70 contractions/min, 2–4% strain), with power initially equal under both conditions. The effect of declining Po2 on power was similar under both conditions but was temperature and tissue dependent. In ventricular trabeculae at 10°C (and atria at 20°C), shortening power declined across the full range of Po2 studied, whereas the power required to lengthen the muscle was unaffected. Conversely, in ventricular trabeculae at 20°C, there was no decline in shortening power but an increase in lengthening power when Po2 fell below 100% air saturation. Finally, when ventricular trabeculae were paced at rates of up to 115 contractions/min at 20°C (vs. the maximum of 70 contractions/min in vivo), they showed marked increases in both shortening and lengthening power. Our results suggest that although elevated heart rates may not impair ventricular power as they commonly do isometric force, limited atrial power and the increased work required to expand the ventricle during diastole may compromise ventricular filling and hence, stroke volume in Atlantic cod at warm temperatures. Neither large strains nor high contraction rates convey an apparent advantage in circumventing this.

scholarly journals Fractal Analysis of Right Ventricular Trabeculae in Pulmonary Hypertension

Radiology ◽  
2018 ◽  
Vol 288 (2) ◽  
pp. 386-395 ◽  
Author(s):  
Timothy J. W. Dawes ◽  
Jiashen Cai ◽  
Marina Quinlan ◽  
Antonio de Marvao ◽  
Philip J. Ostrowski ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Fractal Analysis ◽  
Ventricular Trabeculae

Unloaded shortening velocity of skinned rat myocardium: effects of volatile anesthetics

1990 ◽  
Vol 259 (4) ◽  
pp. H1118-H1125 ◽  
Author(s):  
J. S. Herland ◽  
F. J. Julian ◽  
D. G. Stephenson
Keyword(s):  
Isometric Force ◽  
Dose Dependence ◽  
Test Method ◽  
Dose Response Relationship ◽  
Shortening Velocity ◽  
Velocity Of Shortening ◽  
Cross Bridges ◽  
Dose Levels ◽  
Ventricular Trabeculae ◽  
Unloaded Velocity

The slack test method has been adapted for measurement of unloaded velocity of shortening in rat ventricular trabeculae that were skinned with saponin (50 micrograms/ml for 30 min). The method was sensitive enough to detect a 17% reversible change in the unloaded velocity of shortening produced by a 3 degrees C change in temperature. At pCa 5.30 (80-90% activation), halothane, enflurane, and isoflurane each slowed the shortening velocity by 25-30% at dose levels of 8 mM or greater but not at 4 mM or less. At pCa 5.48 (50-60% activation), halothane slowed the shortening velocity by 20-45% at dose levels of 4 mM or greater but not at 2 mM. The slowing effect of anesthetics on shortening velocity showed saturation at 8 mM for halothane, enflurane, and isoflurane when activation was at pCa 5.30. Saturation occurred at 4 mM for halothane when the pCa was 5.48. This result indicates that the dose-response relationship may be narrow, such that it can be demonstrated between 2 and 4 mM halothane for pCa 5.48 and between 4 and 8 mM halothane for pCa 5.30. The anesthetic dose dependence of isometric force and length axis intercept did not generally follow the same relationship as for the shortening velocity. Thus in several instances force did not significantly decrease when the velocity of shortening did. This may be interpreted as lack of simple inhibition by anesthetics on the number of interacting cross-bridges and as direct influence by anesthetics on the cross-bridge cycle.

Modification of temperature dependence of myofilament Ca sensitivity by troponin C replacement

1990 ◽  
Vol 258 (2) ◽  
pp. C282-C288 ◽  
Author(s):  
S. M. Harrison ◽  
D. M. Bers
Keyword(s):  
Temperature Dependence ◽  
Rat Heart ◽  
Cardiac Tissue ◽  
Mean Shift ◽  
Troponin C ◽  
Native State ◽  
Maximal Tension ◽  
Fast Twitch ◽  
Ventricular Trabeculae ◽  
Ca Sensitivity

The Ca sensitivity of chemically skinned right ventricular trabeculae from the rat heart was determined at 22 and 8 degrees C. Endogenous troponin C (TnC) was then extracted with EDTA and replaced with either bovine cardiac TnC or rabbit fast-twitch skeletal TnC. The temperature dependence of myofilament Ca sensitivity was then reevaluated. Cooling native cardiac tissue from 22 to 8 degrees C reduced the pCa (-log10 [Ca2+]), generating half-maximal tension (K1/2) from 5.20 +/- 0.07 to 4.89 +/- 0.08 (SD, n = 14), and also reduced maximum Ca-activated force to 33 +/- 6% of its value at 22 degrees C. After extraction of endogenous TnC and reconstitution with cardiac TnC, cooling from 22 to 8 degrees C caused a similar shift in mean K1/2 from 4.93 +/- 0.08 to 4.69 +/- 0.06 (n = 7). When skeletal TnC was reconstituted into TnC-extracted ventricular fibers, cooling from 22 to 8 degrees C led to a much smaller mean shift in K1/2 from 4.88 +/- 0.07 to 4.78 +/- 0.04 (n = 7). The results show that the magnitude of the cooling-induced shift in myofilament Ca sensitivity observed in the native state (or after reconstitution with cardiac TnC) is significantly reduced if the fiber is reconstituted with skeletal TnC (P less than 0.001). This indicates that the temperature dependence of myofilament Ca sensitivity of cardiac muscle can be modified by incorporation of skeletal TnC. Thus Ca binding to TnC plays an important role in determining the temperature dependence of myofilament Ca sensitivity.

Effects of halothane on [Ca2+]i transient, SR Ca2+ content, and force in intact rat heart trabeculae

1998 ◽  
Vol 274 (1) ◽  
pp. H106-H114 ◽  
Author(s):  
Yandong Jiang ◽  
Fred J. Julian
Keyword(s):  
High Dose ◽  
Inotropic Action ◽  
Contractile System ◽  
Intracellular Ca ◽  
Butanedione Monoxime ◽  
High Doses ◽  
Versus Peak ◽  
Relationship Of ◽  
The Relationship ◽  
Ventricular Trabeculae

The goal of this study was to test whether the well-known cardiodepressant effect of halothane is caused mainly by depression of the transient increase in intracellular Ca2+ concentration ([Ca2+]i) during a twitch. Intact rat ventricular trabeculae, paced at 0.5 Hz and 30°C with a bathing extracellular Ca2+ concentration ([Ca2+]o) of 2 mM, were used. The [Ca2+]iwas monitored with the use of fura 2 injected into the myoplasm. The sarcoplasmic reticulum (SR) Ca2+content was estimated with the use of rapid cooling (RC)-induced contracture force and Ca2+release. The relationship of the peak [Ca2+]itransient versus peak twitch force obtained with halothane is intermediate between those obtained with lowered [Ca2+]oand varying doses of 2,3-butanedione monoxime. The data indicate that the negative inotropic action of halothane at low (0.18 mM) dose is mainly achieved by reduction in the Ca2+ sensitivity of the contractile apparatus, whereas, at high dose (0.55 mM), halothane acts both by reducing the [Ca2+]itransient and the Ca2+ sensitivity of the contractile system. At moderate (0.37 mM) dose, the effects were midway between low and high doses. With the use of RC contracture force alone, the reduction of SR Ca2+content caused by halothane is overestimated.

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